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Maintenance ECT for treatment of therapy-resistant paranoid schizophrenia and Parkinson's disease
N
CASE REPORT iii
Maintenance ECT for Treatment of Therapy-Resistant Paranoid Schizophrenia and Parkinson' s Disease Gereon H6flich, Siegfried Kasper, Karl-Werner Burghof, Hans-Peter Scholl, and Hans-Jtirgen M611er Key W o r d s :
Electroconvulsive therapy (ECT), paranoid schizophrenia, Parkinson's disease
Introduction Paranoid-hallucinatory symptoms associated with Parkinson's disease create a difficult therapeutic problem, since neuroleptics may exacerbate parkinsonian symptoms, and anti-parkinsonian drugs may aggravate the psychotic syndrome. Electroconvulsive therapy (ECT) has been reported to be helpful in many patients with Parkinson's disease receiving this therapy for a variety of psychiatric indications, including depression, mania, and drug-induced psychosis (Rasmussen and Abrams 1991, 1992). Furthermore, ECT has been reported to be effective in schizophrenic patients with neuroleptic-induced parkinsonism with improvement in both their schizophrenic and parkinsonian symptomatoiogy (Goswami et al 1989). The following report considers a case of ECT to a patient who manifested both sets of symptoms.
Case Report A 49-year-old, right-handed Caucasian woman with a history of severe, therapy-resistant chronic, paranoid-hallucinatory schizophrenia for 26 years and coexisting Parkinson's disease for 11 years was admitted to the Psychiatric Department of the University of Bonn following a progressive deterioration of her physical, neurological, and psychiatric state, including severe social withdrawal. The patient was adequately orientated and manifested an obvious slowness in thinking and speech. She did not consent to an extensive neuropsychological assessment. She presented delusions of guilt, auditory hallucinations of God talking to her and holy persons giving commands, complaints of fatigue, difficulty in From the Psychiatric Department of the University of Bonn. Bonn. Germany. Address reprint requests to Dr, med. G. Hrflich, Psychiatric Department, of the University of Bonn, D-53105 Bonn, Sigmund Freudstr. 25, F.R.G. Received January 10, 1994; revised November 11. 1994.
© 1995 Society of Biological Psychiatry
concentration, and a lack of interest in daily activities. Her mood was mildly depressed with short episodes of subjective tension and anxiety. Her sister may have suffered from a psychotic disorder, and there was no history of Parkinson's disease in the family. Two psychiatrists diagnosed the patient as suffering from chronic paranoid schizophrenia according to DSM-III-R (295.32) (APA 1987). Furthermore, she suffered from severe parkinsonian symptoms consisting of a general akinesia, parkinsonian tremor, cogwheel rigidity of her extremities, bradydiadochokinesia, masked facies, micrographia, seborrhea, speech retardation, and a small stepped gait. Symptoms of dyskinesia were not present. Although the onset of parkinsonian symptoms at the age 38 is considered early, and the comorbidity of schizophrenic psychosis and Parkinson's disease is uncommon, we believe the latter diagnosis to be correct. Previous unsuccessful treatments for both her schizophrenia and Parkinson's disease included medications mostly in combination, such as haloperidol, triperidol, flupenthixol, fluphenazine, clozapine, risperidone, perazine, zotepine, remoxipride, thioridazine, amantadine, deprenyl, L-dopa + decarboxylase inhibitor, biperidene, and metixene. Recommendations to initiate ECT had been rejected earlier by the patient and her husband. At the time of consent for ECT she had been taking haioperidol (8 mg/day), thioridazine (90 mg/day), metixene (17,5 mg/day), and biperidene (6 mg/day). These therapies continue during ECT. The electrocardiogram, electroencephalogram, and blood parameters were normal. The cranial computed tomography detected an unspecific discrete atrophy, especially frontotemporally. ECT was given after inducing anesthesia by an intravenous injection of methohexital (110-190 mg) and obtaining muscle relaxation with succinylcholine (80 mg). Oxygen was administered before and after treatment. Convulsions were induced using a Thymatron device (brief pulses of constant current 0.9 ~, with a pulse frequency of 70 Hz). The energy of the stimulation was dependent on 0006-3223/95/$09.50 SSDI 0006-3223(94)00366-B
Case Report
BIOLPSYCHIATRY
893
1995;37:892-894
WRS total score
pairment nor any other form of organic brain syndrome were observed during the course of inpatient or outpatient maintenance ECT.
30/
25
Discussion 20
15
10
IlllIlll,II, 0
,I,
10 20 30 40 50 60 70 80 90 100 110 120 130 140 150 160 170 180
days inpatient
outpatient
Figure 1. Total scores of the Webster Rating Scale (WRS) during 10 electroconvulsive therapy (ECT) sessions (inpatient) and during five maintenance ECT sessions (outpatient) in a patient with coexisting paranoid schizophrenia and Parkinson's disease. the motor seizure duration measured with the "cuff technique" at the right forearm, and each seizure lasted at least 20 seconds. Because of a reduction of the seizure duration during the course of the ECT sessions, the energy utilized was elevated from 252-504 mC, and electrode placement was changed after the seventh ECT session from the unilateral right side (d'Elia position) to a bilateral frontotemporal position. After clinical improvement and discharge from hospital, maintenance ECT was given every 4 weeks for 5 months, because the patient had rejected being treated at 3- or 2-week intervals. The schedule on a monthly basis has been described in recent literature (Abrams 1992). Psychopathology was rated with the Brief Psychiatric Rating Scale (BPRS) (Overall and Gorham 1976); parkinsonian symptoms were rated using the Webster Rating Scale (WRS) (Webster 1968) at days 0, 1,7.8, 15, 16, 23, and 24. During maintenance ECT, both scales were rated two times a month. During the course of ECT, the parkinsonian symptoms, especially akinesia, improved considerably. The patient could walk with large steps, and speech problems disappeared. After 10 ECT sessions, there was a decrease from 23 to 14 points in the WRS (Figure 1) and a reduction from 48 to 36 points in the total score of the BPRS (Figure 2). The paranoid and hallucinatory symptoms also improved. "Voices" no longer gave commands, and the religious delusions lessened in intensity. With the improvement of her neurological and psychiatric condition, the patient was discharged to her home, and not to a geriatric facility, which had been considered before giving ECT. She also agreed to outpatient maintenance ECT on a monthly basis, which was carried out while the medication was kept constant. Her parkinsonian symptoms fluctuated, but generally did not deteriorate, during the treatment period lasting 5 months (Figure 1). In contrast, per psychotic symptoms fluctuated much more, and there was only little improvement in the BPRS under this treatment regime (Figure 2). Both figures showed treatment days not associated with improvement in BPRS or WRS. Therefore, the possibility of better improvement by ECT given more frequently cannot be excluded. Neither cognitive ira-
During the course of this patient's ECT treatment, the paranoidhallucinatory psychosis as well as the Parkinson's symptomatology improved and then remained stable under maintenance ECT for 5 months. There was more improvement in the latter symptomatology--an effect that is not surprising, considering reports that patients with chronic schizophrenia benefit little from ECT (Abrams 1992) whereas parkinsonian symptoms may improve (Fink 1988; Rasmussen and Abrams 1991). While the mechanism of action of ECT is not known, its efficacy in Parkinson's disease may be explained by an enhancement of centrencephalic dopaminergic activity, which seems well established (Mann and Kapur 1991). Decreased dopamine-autoreceptor sensitivity (Chiodo and Antelman 1987) or increased responsiveness of postsynaptic dopamine receptors (Balldin et al 1981; Andersen et al 1980) have been suggested to be responsible for this effect. On the other hand, however, the dopamine-hypothesis of schizophrenia (Carlsson 1988) postulates a dopaminergic hyperactivity in schizophrenic patients with paranoid-hallucinatory symptomatology which is reduced after successful treatment. Thus it would appear that the improvement of both the parkinsonian and schizophrenic symptoms in this patient casts doubt on the worth of the dopamine hypothesis of schizophrenia. In conclusion, the treatment response in this patient justifies the use of ECT in patients suffering from both a paranoid-hallucinatory syndrome and Parkinson's disease, especially because these patients are difficult to treat with drugs alone due to the antagonizing effects of neuroleptics and dopaminergic agents. Furthermore, maintenance ECT may stabilize the positive response attained.
BPRS total score 60
55
50
45
40
35
30
Itlltlll
I
1
I
l
l
10 20 30 40 50 60 70 80 90 100 110 120 130 140 150 160 170 180
days inpatient
outpatient
Figure 2. Total scores of the Brief Psychiatric Rating Scale (BPRS) during 10 electroconvulsive therapy (ECT) sessions (inpatient) and during five maintenance ECT sessions (outpatient) in a patient with coexisting paranoid schizophrenia and Parkinson's disease.
894
BIOL PSYCHIATRY 1995;37:892-894
Case Report
References Abrams R (1992): Electroconvulsive Therapy, 2nd ed. New York, Oxford: Oxford University Press. American Psychiatric Association ( 1987): Diagnostic and Statistical Manual of Mental Disorders, 3rd ed rev. Washington DC: American Psychiatric Association. Andersen K, Balldin J, Gottfries CG, et al (1987): A double-blind evaluation of electroconvulsive therapy in Parkinson's disease with "on-off" phenomena. Acta Neurol Scand 76:191-199. Balldin J, Eden S, Granerus AK, et al (1981): Electroconvulsive therapy in Parkinson's syndrome with "on-off'' phenomenon. J Neural Transm 47:11-21. Carlsson A (1988): The current state of the dopamine hypothesis of schizophrenia. Neuropsychopharmacology 1: 179-186. Chiodo LA, Antelmann SM (1980)- Electroconvulsive shock: Progressive dopamine autoreceptor subsensitivity independent of repeated treatment. Science 210:799-801. Fink M (1988): ECT for Parkinson'disease? (Editorial.) Convul Ther4:189-191.
Goswami U, Dutta S, Kuruvilla K, Papp E, Perenyi A (1989): Electroconvulsive therapy in neuroleptic-induced Parkinsonism. Biol Psychiatry 26:234-238. Mann J J, Kapur S (1991): Neurobiological mechanisms of ECT: Clinical studies. In Racagni G, Brunnelo N, Fukuda T (eds), Biological Psychiatry. Amsterdam, London, New York, Tokyo: Excerpta Medica, pp 272-274. Overall JE, Gorham DR (1976): BPRS Brief Psychiatric Rating Scale. In: Guy W (ed) ECDEU Assessment manual for psychopharmacology, rev edn, Rockville, Maryland pp 157-169. Rasmussen KG, Abrams R (1991): Treatment of Parkinson' s disease with electroconvulsive therapy. Psychiat Clin North Am 14:925-933. Rasmussen KG, Abrams R (1992): The role of electroconvulsive therapy in Parkinson's disease. In Huber S, Cummings J (eds), Neurobehavioral Aspects of Parkinson "s disease. New York: Oxford University Press, pp 252-270. Webster DD (1968): Critical analyses of the disability in Parkinson' s disease. Med Treat 5:257-282.
CASE REPORT iii
Maintenance ECT for Treatment of Therapy-Resistant Paranoid Schizophrenia and Parkinson' s Disease Gereon H6flich, Siegfried Kasper, Karl-Werner Burghof, Hans-Peter Scholl, and Hans-Jtirgen M611er Key W o r d s :
Electroconvulsive therapy (ECT), paranoid schizophrenia, Parkinson's disease
Introduction Paranoid-hallucinatory symptoms associated with Parkinson's disease create a difficult therapeutic problem, since neuroleptics may exacerbate parkinsonian symptoms, and anti-parkinsonian drugs may aggravate the psychotic syndrome. Electroconvulsive therapy (ECT) has been reported to be helpful in many patients with Parkinson's disease receiving this therapy for a variety of psychiatric indications, including depression, mania, and drug-induced psychosis (Rasmussen and Abrams 1991, 1992). Furthermore, ECT has been reported to be effective in schizophrenic patients with neuroleptic-induced parkinsonism with improvement in both their schizophrenic and parkinsonian symptomatoiogy (Goswami et al 1989). The following report considers a case of ECT to a patient who manifested both sets of symptoms.
Case Report A 49-year-old, right-handed Caucasian woman with a history of severe, therapy-resistant chronic, paranoid-hallucinatory schizophrenia for 26 years and coexisting Parkinson's disease for 11 years was admitted to the Psychiatric Department of the University of Bonn following a progressive deterioration of her physical, neurological, and psychiatric state, including severe social withdrawal. The patient was adequately orientated and manifested an obvious slowness in thinking and speech. She did not consent to an extensive neuropsychological assessment. She presented delusions of guilt, auditory hallucinations of God talking to her and holy persons giving commands, complaints of fatigue, difficulty in From the Psychiatric Department of the University of Bonn. Bonn. Germany. Address reprint requests to Dr, med. G. Hrflich, Psychiatric Department, of the University of Bonn, D-53105 Bonn, Sigmund Freudstr. 25, F.R.G. Received January 10, 1994; revised November 11. 1994.
© 1995 Society of Biological Psychiatry
concentration, and a lack of interest in daily activities. Her mood was mildly depressed with short episodes of subjective tension and anxiety. Her sister may have suffered from a psychotic disorder, and there was no history of Parkinson's disease in the family. Two psychiatrists diagnosed the patient as suffering from chronic paranoid schizophrenia according to DSM-III-R (295.32) (APA 1987). Furthermore, she suffered from severe parkinsonian symptoms consisting of a general akinesia, parkinsonian tremor, cogwheel rigidity of her extremities, bradydiadochokinesia, masked facies, micrographia, seborrhea, speech retardation, and a small stepped gait. Symptoms of dyskinesia were not present. Although the onset of parkinsonian symptoms at the age 38 is considered early, and the comorbidity of schizophrenic psychosis and Parkinson's disease is uncommon, we believe the latter diagnosis to be correct. Previous unsuccessful treatments for both her schizophrenia and Parkinson's disease included medications mostly in combination, such as haloperidol, triperidol, flupenthixol, fluphenazine, clozapine, risperidone, perazine, zotepine, remoxipride, thioridazine, amantadine, deprenyl, L-dopa + decarboxylase inhibitor, biperidene, and metixene. Recommendations to initiate ECT had been rejected earlier by the patient and her husband. At the time of consent for ECT she had been taking haioperidol (8 mg/day), thioridazine (90 mg/day), metixene (17,5 mg/day), and biperidene (6 mg/day). These therapies continue during ECT. The electrocardiogram, electroencephalogram, and blood parameters were normal. The cranial computed tomography detected an unspecific discrete atrophy, especially frontotemporally. ECT was given after inducing anesthesia by an intravenous injection of methohexital (110-190 mg) and obtaining muscle relaxation with succinylcholine (80 mg). Oxygen was administered before and after treatment. Convulsions were induced using a Thymatron device (brief pulses of constant current 0.9 ~, with a pulse frequency of 70 Hz). The energy of the stimulation was dependent on 0006-3223/95/$09.50 SSDI 0006-3223(94)00366-B
Case Report
BIOLPSYCHIATRY
893
1995;37:892-894
WRS total score
pairment nor any other form of organic brain syndrome were observed during the course of inpatient or outpatient maintenance ECT.
30/
25
Discussion 20
15
10
IlllIlll,II, 0
,I,
10 20 30 40 50 60 70 80 90 100 110 120 130 140 150 160 170 180
days inpatient
outpatient
Figure 1. Total scores of the Webster Rating Scale (WRS) during 10 electroconvulsive therapy (ECT) sessions (inpatient) and during five maintenance ECT sessions (outpatient) in a patient with coexisting paranoid schizophrenia and Parkinson's disease. the motor seizure duration measured with the "cuff technique" at the right forearm, and each seizure lasted at least 20 seconds. Because of a reduction of the seizure duration during the course of the ECT sessions, the energy utilized was elevated from 252-504 mC, and electrode placement was changed after the seventh ECT session from the unilateral right side (d'Elia position) to a bilateral frontotemporal position. After clinical improvement and discharge from hospital, maintenance ECT was given every 4 weeks for 5 months, because the patient had rejected being treated at 3- or 2-week intervals. The schedule on a monthly basis has been described in recent literature (Abrams 1992). Psychopathology was rated with the Brief Psychiatric Rating Scale (BPRS) (Overall and Gorham 1976); parkinsonian symptoms were rated using the Webster Rating Scale (WRS) (Webster 1968) at days 0, 1,7.8, 15, 16, 23, and 24. During maintenance ECT, both scales were rated two times a month. During the course of ECT, the parkinsonian symptoms, especially akinesia, improved considerably. The patient could walk with large steps, and speech problems disappeared. After 10 ECT sessions, there was a decrease from 23 to 14 points in the WRS (Figure 1) and a reduction from 48 to 36 points in the total score of the BPRS (Figure 2). The paranoid and hallucinatory symptoms also improved. "Voices" no longer gave commands, and the religious delusions lessened in intensity. With the improvement of her neurological and psychiatric condition, the patient was discharged to her home, and not to a geriatric facility, which had been considered before giving ECT. She also agreed to outpatient maintenance ECT on a monthly basis, which was carried out while the medication was kept constant. Her parkinsonian symptoms fluctuated, but generally did not deteriorate, during the treatment period lasting 5 months (Figure 1). In contrast, per psychotic symptoms fluctuated much more, and there was only little improvement in the BPRS under this treatment regime (Figure 2). Both figures showed treatment days not associated with improvement in BPRS or WRS. Therefore, the possibility of better improvement by ECT given more frequently cannot be excluded. Neither cognitive ira-
During the course of this patient's ECT treatment, the paranoidhallucinatory psychosis as well as the Parkinson's symptomatology improved and then remained stable under maintenance ECT for 5 months. There was more improvement in the latter symptomatology--an effect that is not surprising, considering reports that patients with chronic schizophrenia benefit little from ECT (Abrams 1992) whereas parkinsonian symptoms may improve (Fink 1988; Rasmussen and Abrams 1991). While the mechanism of action of ECT is not known, its efficacy in Parkinson's disease may be explained by an enhancement of centrencephalic dopaminergic activity, which seems well established (Mann and Kapur 1991). Decreased dopamine-autoreceptor sensitivity (Chiodo and Antelman 1987) or increased responsiveness of postsynaptic dopamine receptors (Balldin et al 1981; Andersen et al 1980) have been suggested to be responsible for this effect. On the other hand, however, the dopamine-hypothesis of schizophrenia (Carlsson 1988) postulates a dopaminergic hyperactivity in schizophrenic patients with paranoid-hallucinatory symptomatology which is reduced after successful treatment. Thus it would appear that the improvement of both the parkinsonian and schizophrenic symptoms in this patient casts doubt on the worth of the dopamine hypothesis of schizophrenia. In conclusion, the treatment response in this patient justifies the use of ECT in patients suffering from both a paranoid-hallucinatory syndrome and Parkinson's disease, especially because these patients are difficult to treat with drugs alone due to the antagonizing effects of neuroleptics and dopaminergic agents. Furthermore, maintenance ECT may stabilize the positive response attained.
BPRS total score 60
55
50
45
40
35
30
Itlltlll
I
1
I
l
l
10 20 30 40 50 60 70 80 90 100 110 120 130 140 150 160 170 180
days inpatient
outpatient
Figure 2. Total scores of the Brief Psychiatric Rating Scale (BPRS) during 10 electroconvulsive therapy (ECT) sessions (inpatient) and during five maintenance ECT sessions (outpatient) in a patient with coexisting paranoid schizophrenia and Parkinson's disease.
894
BIOL PSYCHIATRY 1995;37:892-894
Case Report
References Abrams R (1992): Electroconvulsive Therapy, 2nd ed. New York, Oxford: Oxford University Press. American Psychiatric Association ( 1987): Diagnostic and Statistical Manual of Mental Disorders, 3rd ed rev. Washington DC: American Psychiatric Association. Andersen K, Balldin J, Gottfries CG, et al (1987): A double-blind evaluation of electroconvulsive therapy in Parkinson's disease with "on-off" phenomena. Acta Neurol Scand 76:191-199. Balldin J, Eden S, Granerus AK, et al (1981): Electroconvulsive therapy in Parkinson's syndrome with "on-off'' phenomenon. J Neural Transm 47:11-21. Carlsson A (1988): The current state of the dopamine hypothesis of schizophrenia. Neuropsychopharmacology 1: 179-186. Chiodo LA, Antelmann SM (1980)- Electroconvulsive shock: Progressive dopamine autoreceptor subsensitivity independent of repeated treatment. Science 210:799-801. Fink M (1988): ECT for Parkinson'disease? (Editorial.) Convul Ther4:189-191.
Goswami U, Dutta S, Kuruvilla K, Papp E, Perenyi A (1989): Electroconvulsive therapy in neuroleptic-induced Parkinsonism. Biol Psychiatry 26:234-238. Mann J J, Kapur S (1991): Neurobiological mechanisms of ECT: Clinical studies. In Racagni G, Brunnelo N, Fukuda T (eds), Biological Psychiatry. Amsterdam, London, New York, Tokyo: Excerpta Medica, pp 272-274. Overall JE, Gorham DR (1976): BPRS Brief Psychiatric Rating Scale. In: Guy W (ed) ECDEU Assessment manual for psychopharmacology, rev edn, Rockville, Maryland pp 157-169. Rasmussen KG, Abrams R (1991): Treatment of Parkinson' s disease with electroconvulsive therapy. Psychiat Clin North Am 14:925-933. Rasmussen KG, Abrams R (1992): The role of electroconvulsive therapy in Parkinson's disease. In Huber S, Cummings J (eds), Neurobehavioral Aspects of Parkinson "s disease. New York: Oxford University Press, pp 252-270. Webster DD (1968): Critical analyses of the disability in Parkinson' s disease. Med Treat 5:257-282.